The first neuromuscular disorder for which plasma exchange was suggested as a treatment was myasthenia gravis. Since that time, plasma exchange has been attempted on several other neurological diseases, including Eaton-Lambert myasthenic syndrome, polymyositis, dermatomyositis, acute Guillain-Barre syndrome, chronic Guillain-Barre syndrome, multiple sclerosis, Refsum's disease, Amyotrophic lateral sclerosis, hyperviscosity coma, and polyneuropathy. Results have for various of these treatments have been characterized as positive, equivocal, doubtful, and negative. See P. Reuther, Plasma Exchange Therapy in Neurological Disorders: A Clinician's Overview, in Therapeutic Hemapheresis, vol. 2, pgs 27-54 (J. MacPherson and D. Kasprisin Eds. 1985); see also Current Practices in Therapeutic Plasmapheresis, pgs 158-177 (Y. Shiokawa and N. Inoue Eds. 1985); Therapeutic Apheresis, pgs. 35-58 (J. Kolins and J. Jones Eds. 1983); H. Weiner, Science 259, 1321 (26 Feb. 1993).
For myasthenia gravis, it is generally accepted that anti-acetylcholine receptor antibodies are the underlying pathologic factors which are removed by plasma exchange. For most of the other nervous system diseases treated by plasma exchange, the underlying etiology is unknown. However, without a knowledge of the underlying mechanism of the disease, it is difficult to monitor antibody levels in conjunction with plasma exchange so that treatment may be appropriately administered. Accordingly, there is a continued need for greater understanding of the autoimmune mechanisms underlying nervous system disorders.